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1-adrenoceptor blockade promotes growth of arterioles and preserves coronary perfusion reserve in post-infarcted heart
1 Department of Anatomy and Cell Biology, University of Iowa Carver College of Medicine, Iowa City, Iowa, USA
2 Department of Internal Medicine, University of Iowa Carver College of Medicine, Iowa City, Iowa, USA; The Cardiovascular Center, University of Iowa Carver College of Medicine, Iowa City, Iowa, USA; Department of Veterans Affairs Medical Center, University of Iowa Carver College of Medicine, Iowa City, Iowa, USA
3 Department of Anatomy and Cell Biology, University of Iowa Carver College of Medicine, Iowa City, Iowa, USA; The Cardiovascular Center, University of Iowa Carver College of Medicine, Iowa City, Iowa, USA
* To whom correspondence should be addressed. E-mail: eduard-dedkov{at}uiowa.edu.
Adequate growth of coronary vasculature in the remaining LV myocardium of post-MI heart is a crucial factor for myocyte survival and performance. We have previously demonstrated that post-infarcted coronary angiogenesis can be stimulated by bradycardia induced with the KATP channel antagonist alinidine. In this study we tested the hypothesis that heart rate reduction with 
1-blockade may also induce coronary growth in post-MI heart. Transmural MI was induced in 12-month-old male Sprague-Dawley rats by occlusion of the LAD coronary artery. Bradycardia was induced by administering the 1-adrenoceptor blocker atenolol (AT) via drinking water (30 mg/day). Three groups of rats were compared: 1) control/sham (C/SH), 2) MI, 3) MI +AT. In the AT-treated post-MI rats, heart rate was consistently reduced by 25-28% compared to C/SH rats. Four weeks after LAD artery ligation infarct size was similar in MI and MI+AT rats (67.1% and 61.5%, respectively), whereas a greater ventricular hypertrophy occurred in bradycardic rats, as indicated by a higher ventricular/body weight ratio (3.4±0.1 vs. 2.8±0.1 mg/g in MI rats). The analysis of LV function revealed that the MI+AT group had a smaller drop in ejection fraction than the untreated MI group (~24% vs. ~35%). Furthermore, in MI+AT rats, both maximal coronary conductance and coronary perfusion reserve were significantly improved compared to those in untreated post-MI group. The better myocardial perfusion indices in MI+AT rats were associated with a greater increase in arteriolar length density than detected in the untreated MI group. Thus, chronic reduction of heart rate induced with 1-selective blockade promotes growth of coronary arterioles and, thereby, facilitates regional myocardial perfusion in post-MI hearts.
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